Voluntary exercise has been demonstrated to have ATD-like effects in animal models of depression. The enhancement of GF signaling may be one possible mechanism that can account for these ADT-like effects as exercise has been demonstrated to increase neurotrophic factors such as brain derived neurotrophic factor (BDNF). To further characterize the neruotrophic actions of exercise we have synthesized our own custom GF coda microarray chip. In these studies, we compare individual animals by first isolating total RNA from each animal and reverse transcribing into coda using Cy3 and Cy5 primers for sedentary and exercise animals respectively. Before analysis, samples were normalized to housekeeping genes. From these arrays we have found various neurotrophic factors to be regulated by exercise. We have focused on one of these exercise regulated genes, VGF (nonacronymic) and confirmed its regulation by in situ hybridization in addition to determining it can produce ADT-like effects in an animal model of depression, the FST, when infused into either the hippocampus (in rats) or the lateral ventricles (in mice). We are now in the process of determining the effects of VGF on neurogenesis.